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In recent years, studies have shown that supplementation of omega 3 fatty acids (n-3 PUFA) could be associated with increased rates of muscle protein synthesis, and may contribute to the greater gain in muscle mass and strength chronically. However, unlike studies with older adults, studies in young adults are contradictory, and while some observe greater gains in muscle mass and strength in response to n-3PUFA supplementation in healthy adults, others do not demonstrate these effects. The aim of this systematic review is to evaluate the current evidence of the efects of n-3pUFA supplementation on muscle mass and strenght in adults.

Bone is a plastic tissue, and is responsive to exercise intervention, but currently little is known about how various exercise and participant characteristics interact to influence bone metabolism. Acute, controlled, interventions provide an in-vivo model through which the acute bone response to exercise-based stimuli can be investigated, and these are typically monitored using circulating bone biomarkers. Currently, substantial heterogeneity in factors such as study design, quality, exercise and participant characteristics render it difficult to synthesize and evaluate the available evidence. We will conduct a systematic review and meta-analysis to investigate the bone biomarker response to an acute bout of exercise, including examination of potential moderating factors, e.g., variation in participant and exercise characteristics.

Evidence indicates that low energy availability may impair bone metabolism. Little is currently known, however, about the mechanisms via which this occurs, nor whether strategies such as varying the macronutrient composition of the diet may be effective in attenuating these effects. The aim of the current study is to investigate the influence of a brief period of low energy availability, with varying protein compositions, on the bone biomarker response to an acute bout of exercise.

Dynamic and acute responses of bone (re)modelling to exercise bouts can be investigated by using bone biochemical markers of bone resorption (such as β-CTX-1) and formation (such as P1NP). There are, however, a number of issues that potentially limit the use and the interpretations that can be made from these markers, such as variability derived from pre-analytical (e.g., markers' circadian rhythms) and analytical (e.g., laboratory assays) factors. The estimation of typical error would allow quantification of the degree to which the observed changes in bone (re)modelling markers are affected by measurement error caused by factors, such as laboratory assays and circadian rhythms; and assessing the intervention response variation would enable researchers to determine if concentration changes across individuals are directly caused by the intervention of interest. Whilst obtaining accurate estimates of all of these variability assessments is difficult for single studies, meta-analytic approaches can counteract limitations of small effects, noisy measurement outcomes and small sample sizes. Individual participant data (IPD) meta-analyses provide better estimates of mean responses, allow for the assessment of effects at the participant level by using the raw data from selected studies. Therefore, the aims of this investigation are (i) to evaluate the mean responses of reference bone (re)modelling markers β-CTX-1 and P1NP after a prolonged, continuous running exercise bout in young adult males, (ii) to estimate the inter-individual variation in bone (re)modelling marker responses and (iii) to determine to what degree this inter-individual variation was caused by factors directly related to the prolonged continuous running bout (herein termed the intervention response) or by external factors (e.g., circadian variation). Thus, we will use a combined approach of aggregate data and individual participant data systematic review and meta-analysis.

A better understanding of symptom presentation (both acute and chronic) in athletes is essential to inform safe return to sport decision making and guidelines, as well as to allow for adequate screening and monitoring of potentially at-risk athletes. As such, the aim of the current study is to conduct a systematic review of evidence regarding symptom presentation (acute and persistent) in athletes.

The long-term performance of medical implants is hindered by the foreign body response (FBR). This protective mechanism is intended to isolate potentially harmful objects from the body. Ultimately, inflammatory cytokines such as TGF-β1 activate myofibroblasts, which deposit a hypo-permeable, collagen-rich fibrotic capsule (FC). This is problematic for implants designed for therapy delivery as the FC impedes molecular exchange. We previously reported that intermittent pneumatic actuation (IA) of an implanted reservoir can significantly reduce FC thickness in a 14-day rat model1. Recently, we impressively demonstrated that insulin diffusion kinetics were maintained at baseline levels for the entire eight-week study in a mouse model when implanted reservoirs received IA2. We hypothesise that actuation-induced tissue strain can modulate local inflammatory pathways: to investigate this, we examine cellular interactions that modulate collagen production under IA in vitro. Myofibroblasts (WPMY-1) were seeded onto reservoirs and cultured for 14 days under IA. Cell viability was evaluated using metabolic activity and cytotoxicity assays. Collagen (Sircol Soluble Collagen assay) and TGF-β1 (ELISA) production were compared to non-actuated controls. Analytical models of device strain were developed based on Von Kármán plate theory. We observed that IA did not negatively affect cell viability. Interestingly, IA induced a significant reduction (p=0.0463) in TGF-β1 production, followed by a significant reduction in collagen production after 9 (p=0.0132) and 14 (p=0.0038) days actuation compared to non-actuated controls. Models predict maximum radial and tangential strains of 3.9% during IA. We have demonstrated the compelling potential of IA to modulate the FBR, optimising the local implant environment for therapy diffusion1,2. In vitro, we have uncovered alterations in the TGF-β1 pathway leading to a reduction in collagen production by WPMY-1 cells exposed to IA. Ongoing work is investigating a wider range of inflammatory markers, and correlating strain predictions to cell and tissue responses to fully elucidate the mechanism of IA mediated FBR modulation.